INFLAMMATION Complex reaction in the vascularized connective tissue brought about by exogenous and endogenous stimuli. Fundamentally a protective response the ultimate goal of which is to get rid of the organism

3 MAJOR COMPONENTS OF ACUTE INFLAMMATION Alteration in vascular caliber that lead to an increase in blood flow. Structural changes in microvasculature that permit the plasma proteins and leukocytes to leave the circulation. Emigration of leukocyte from the microcirculation and their accumulation in the focus of injury.

PHAGOCYTOSIS Recognition and attachment of the particle to be ingested by the leukocyte. Engulfment with subsequent formation of the phagocytic vacoule. Killing and degradation of the ingested material.

RECOGNITION OF MICROBES AND DEAD TISSUES Events in the Response of leukocytes:

Recognition of the offending agents Activation of leukocytes to ingest and destroy Receptors for microbial products

H2O2 (lysozomes) + Myeloperoxidase (azurophilic granules of neutrophils) in the presence of Cl- = hypochlorite Most efficient bactericidal system in neutrophils H2O2 may also be converted to hydroxyl radical Fungi,viruses, protozoa and helminths

SYSTEMIC EFFECTS OF INFLAMMATION (ACUTE-PHASE RESPONSE) Fever Acute-phase proteins Leukocytosis Other manifestations Sepsis, in severe large amount or in debilitated patientsnts of organisms and LPS in the blood

SYSTEMIC EFFECTS OF INFLAMMATION (ACUTE-PHASE RESPONSE) Fever

Elevation 1 to 4 °C Most prominent Caused by pyrogens resulting to the resetting of the temperature set point

SEROUS INFLAMMATION Marked by outpouring of a thin fluid from the plasma or secreted by mesothelial cells Effusion, accumulation of fluid in cavities Skin blisters from burns

FIBRINOUS INFLAMMATION Fibrin is formed and deposited in the extravascular space Fibrinous exudate is formed if the vascular leak is large or if there is procoagulant stimulus (cancer cells) Characteristic inflammation in the lining cavities: meninges, pericardium and pleura

Removed by fibrinolysis May undergo organization to form scar tissue

SUPPURATIVE/PURULENT INFLAMMATION Production of large amount of pus or purulent exudate consisting of neutrophils, liquefactive necrosis and edema fluid. Acute appendicitis, common example Abscess – localized collection of purulent inflammatory tissue Produced by deep seeding of a pyogenic bacteria into a tissue In time abscess may be walled off and replaced by connective tissue

ULCERS Local defect or excavation of the surface of an organ or tissue that is produced by the sloughing/shedding of inflamed necrotic tissue Occur only when tissue necrosis and inflammation exist on or near a surface Best exemplified by peptic ulcer

OUTCOMES OF ACUTE INFLAMMATION:

Complete resolution Fibrosis When there is substantial tissue destruction, incapable of regeneration fibrin exudation that cannot be adequately cleared Connective tissue grow into the area of damage Progression to Chronic Inflammation

GRANULOMATOUS INFLAMMATION Distinct pattern of chronic inflammatory reaction in which the predominant cell type is an activated macrophage with a modified epithelial appearance Cellular attempt to contain an offending agent Often there is strong activation of T lymphocytes leading to macrophage activation TB is the prototype

GRANULOMA Focal area of a granulomatous inflammation

Microscopic aggregation of macrophages that are transformed into epithelium like cells surrounded by collar of mononuclear leukocytes, lymphocytes and occasionally plasma cells. Rim of fibroblasts & connective tissue Giant cells